Interpretive Summary: Animals are recognized sources for numerous human pathogens, and the animal's feces are a viable route of transmission of the pathogen to environment and human foodstuffs. The intestinal bacterial population is quite complex and the potential for diet to affect these populations and fecal pathogen shedding is poorly understood. Selectively enriching beneficial bacteria, such as the Lactobacillus that can thrive on dietary lactose, is one potential approach to reducing pathogen shedding. Dried skim milk contains 50% lactose and, in growing swine, lactose is poorly absorbed by the animal and should increase Lactobacillus numbers in the feces. Animals consuming 10% dried skim milk in their diet had higher numbers of Lactobacillus, but shedding of pathogens, such as Salmonella and Campylobacter, did not decrease. The benefits of Lactobacillus may have been reduced by higher generic Escherichia coli in the feces of the dried skim milk fed animals. Fecal pathogen shedding was more closely associated with shifts in intestinal bacterial flora as a consequence of changes in feed additives (antimicrobial growth promoters) than the diet per se. Understanding better the intestinal microbial ecology and the effects of production changes on this ecology should provide better control on pathogen shedding by farm animals.

Technical Abstract:
The aims of this study were to determine the possible effect of dried skim milk (DSM) on indigenous Lactobacillus spp. and generic Escherichia coli, and potential for controlling pathogen shedding and affect animal growth in growing-finishing swine. Animals were fed over three dietary phases to match production needs from age 10-14 weeks, 14-18 weeks and 18-22 weeks. For each feeding phase, diets were formulated to contain 0 or 10% DSM (balanced with metabolizable energy and true ileal digestible amino acids). Animals were weighed every two weeks and fecal samples were collected from 40 animals (20 with DSM and 20 without DSM) at week 10 (d 0 on diets), 14, 18 and 22 of age, and were analyzed for Lactobacillus (LB), Enterobacteriaceae (EB), coliforms (CF), generic Escherichia coli (EC), Salmonella, Campylobacter and Escherichia coli O157:H7. At week 10, fecal bacterial counts (log10 CFU/g feces) were 9.55, 7.26, 7.01 and 6.93 for LB, EB, CF and EC populations, respectively. The EB, CF and EC populations decreased through week 14 and 18, but were still higher with the DSM diet. The LB population decreased over time in the absence of DSM in the diet, whereas DSM sustained higher LB counts. At week 22, populations of EB, CF and EC were higher than week 18 for the diet without DSM, but no change was observed with DSM, and no differences between the diets were observed at week 22. However, in week 22 the animal gain was positively correlated with LB numbers and negatively correlated with EC numbers. Subtraction of the EC population (log10) from the LB population (log10) yielded a positive value termed effective LB that correlated well with animal gain and may better define a beneficial function in the intestine. Salmonella were detected in 70% of the animals at week 10 and 14, and less than 20% at week 18 and 22. Campylobacter were detected rarely at weeks 10, 14 and 18, but were found in 25% of the animals at week 22. DSM did not affect Salmonella or Campylobacter shedding, but examination of individual animals over the entire experiment indicated that fewer recurring incidences of Salmonella shedding occurred in animals that maintained higher LB bacteria. In addition, at week 22, Salmonella and Campylobacter shedding was associated with lower levels of effective LB and lower animal wieght gains. We conclude that DSM did not directly affect animal performance or pathogen shedding via the Lactobacillus spp. population at any phase of production. However, analysis of data from all animals revealed that fecal Lactobacillus spp. affected Salmonella shedding and, in the finishing phase, animal growth and pathogen shedding as reflected by the 'effective' Lactobacillus-associated observations. Based on this work, we surmise that benefits from gastrointestinal Lactobacillus spp. in swine may be compromised by the generic Escherichia coli population, and this antagonism may explain poor effects associated with prebiotics or probiotics in some swine studies.